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\begin{document}

\title{Bullous Striae Distensae in a Nephrotic Syndrome Patient: A Case Report
of a Rare Presentation and Review of the Literature}



\author[1]{Sumayyah  Alrefaie}%
\author[1]{Sarah  Aljoudi}%
\author[2]{Houriah  Yasir Nukaly}%
\author[3]{Waseem  AlHawasawi}%
\author[1]{Jehad Hariri}%
\affil[1]{King Abdulaziz University}%
\affil[2]{Batterjee Medical College for Sciences and Technology}%
\affil[3]{King Fahd Armed Forces Hospital}%


\vspace{-1em}



  
  \date{June 15, 2024}


\begingroup
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\textbf{Introduction}

Striae Distensae (SD), a well-recognized phenomenon resulting from
dermal scaring, it is usually associated with physiological conditions
such as pregnancy, growth spurt, rapid weight loss or gain or iatrogenic
causes such as topical or systemic corticosteroid
administration\textsuperscript{1}. It is aesthetically troublesome and
therapeutically challenging. SD early stages appear as flesh-toned
atrophic linear plaques that eventually progress to silvery-whitish
atrophic plaques.\textsuperscript{1,2} Most commonly affect dispensable
body areas such as the buttock, lower back, thighs, calves, breast and
abdomen.\textsuperscript{3} Rare secondary changes within SD have been
mentioned in the literature, including edema, urticaria,
dyspigmentation, ulceration, dehiscence and subcutaneous emphysema.
Fluid filling these striae are an unusual finding. Very few cases have
been reported discussing this phenomenon.\textsuperscript{4,5} Upon
literature review, it was notable that even in the very few case reports
of BSD, almost all the patients were on long-term oral steroids as well
as having hypoalbuminemia, except for one patient as demonstrated
in\emph{Table 1} .\textsuperscript{4} Herein, we report a case of a
17-year-old girl with nephrotic syndrome who was treated with high dose
of corticosteroids presented to the day-care unit with Bullous Striae
Distensae.

\textbf{Literature Review}

\textbf{Table 1:} Main findings from literature review addressing each
of the selected domains.

\textbf{Case Report}

We present a 17-year-old female who was referred to us from the day care
unit for the management of bullous lesions that started to appear on her
abdomen 5 days prior. The patient was known to have Nephrotic syndrome
since the age of 1 year. Initially she had steroid dependent Nephrotic
syndrome for years and had received fluctuating doses of systemic
steroids for a long duration. Later, she was diagnosed with steroid
resistant nephrotic syndrome at the age of 12.

Upon physical examination, she was found to have a cushingoid body
habitus, moon face, central obesity, abdominal striae and ascites. Rapid
weight gain was also noticed recently. There were multiple translucent
bullae along the striae distribution on her abdomen and extending to the
flanks as demonstrated in \emph{Figure 1} . The bullae were tender to
touch and filled with clear fluid.

Latest laboratory investigations showed typical features of nephrotic
syndrome; hypoproteinaemia (total protein 44 g/dL and Albumin 5 g/dL)
and abnormal lipid profile (Total cholesterol 6.9 mmol/L, LDL 4.01
mmol/L and Triglyceride 2.63 mmol/L). Additional laboratory findings
included anaemia (Haemoglobin (Hb) 9.0 g/dL), neutrophilic leucocytosis
(white blood cells 22.1 cells/mm3 and neutrophil 20.48 k/uL),
lymphopenia (1.00 k/uL), thrombocytosis (PLT
541*10\textsuperscript{9}/L), hypocalcaemia (Ca\textsuperscript{2+} 1.91
mmol/L), high microalbumin/creatinine ratio of 10380.9000 mg/g and
abnormal urine analysis (152 RBC / HPF). Fluid aspiration culture and
sensitivity was negative for the presence of bacteria and fungi, fluid
albumin level was 0.3, and white blood cells count was 42
cells\textbackslash{}mm\textsuperscript{3}. Skin punch biopsy of one of
the bullae with haematoxylin and eosin (H and E) stain revealed
oedematous dermis with relatively thinned horizontally oriented dermal
collagen. \emph{Table 2} summarizes the abnormal laboratory results.
These features supported the diagnosis of Bullous Striae Distensae.
Patient was treated with 80 mg Furosemide once daily for 14 days and the
bullae started to disappear slowly without any further intervention.

\textbf{Discussion}

Striae Distensae, are common skin lesions characterized by linear
atrophic plaques directed perpendicularly to the
skin.\textsuperscript{2,4} They represent either, benign physiological
changes as during pregnancy and adolescence, or a pathological sign of
certain diseases.\textsuperscript{4} Rarely, bullae can develop within
the striae.\textsuperscript{5,6,7} They exhibit lower hydration levels
in both the epidermis and dermis, along with reduced dermal echo density
and elasticity compared to normal skin.\textsuperscript{10} A rare
variation of stria distensae, Bullous Stria Distensae, is characterized
by the development of tense bullae within the stria. Almashat et al.
suggested that patients with nephrotic syndrome and chronic steroid use
may trigger bullous stria development, particularly in cases of
anasarca.\textsuperscript{2,7} The pathogenesis of BSD remains
uncertain, however, it has been hypothesized that mechanical stress on
the dermis leads to the rupture of the dermal vasculature and subsequent
bullae formation. Seshadri et al. additionally proposed that the weak
tensile strength of the stria may contribute to the build-up of fluid
within them. Besides, as the size of the stria increases, the likelihood
of fluid accumulation also increases.\textsuperscript{3} Masoud et al.
reported that patients on oral steroids, developing generalized body
edema, tend to accumulate fluid, particularly in the striae. They
further put forward a hypothesis that the phenomenon might result from
the combined effect of both anasarca and steroid medication.
Glucocorticoids were thought to enhance the collagen breakdown, reducing
tensile strength allowing fluid to accumulate preferentially from
anasarca within the stria spaces, forming fluid-filled
sacs.\textsuperscript{5}

In our case, a 17-year-old female with nephrotic syndrome presented with
an emergence of bullous lesions on her abdominal striae. The distinctive
histopathologic characteristics of edematous dermis with a slightly thin
and horizontally oriented dermal collagen confirmed the diagnosis of
BSD. With regard to fluid aspiration culture and sensitivity report, the
bullae were found to be sterile, which is consistent with a previous
report by Seshadri et al.\textsuperscript{3} To the best of our
knowledge, this is the fourth case reported the occurrence of bullous
skin disease in a patient with nephrotic syndrome documented in the
literature. The rapid weight gain and the presence of ascites in our
patient may have resulted in increased mechanical stress on the dermis,
which contributed to the development of BSD. The coexistence of
lipodystrophy and hypoproteinemia in nephrotic syndrome may have further
weakened dermal collagen, potentially increasing the patient's
susceptibility to BSD development.\textsuperscript{2,4} In our case and
other reported cases, patients had hypoalbuminemia due to different
pathologies and striae Distensae. Three of the reported cases were
associated with receiving high or fluctuating dose of systemic steroid
for varying duration.\textsuperscript{2,3,7} This phenomenon can be
explained by the effect of decreased oncotic pressure on weakened or
atrophic layers of skin.\textsuperscript{6} In this clinical context,
differential diagnosis includes autoimmune bullous diseases, which can
be ruled out through direct immunofluorescence. However, managing the
underlying medical illness with diuresis can lead to spontaneous
resolution, as puncture and aspiration of fluids alone would result in
rapid fluid reaccumulation. Jogova et al. also highlighted that upon
treatment with diuresis, flattening of the fluid-filled stria were
notable.\textsuperscript{4} Certainly, BSD management is primarily
centred around addressing the underlying cause. In our case, the
administration of diuretics to manage her ascites played a role in
reducing the mechanical stress on the dermis, which resulted in a
gradual resolution of the bullae. The strength of our case report lies
in its rarity, as we are only the second case report highlighting the
potential advantage of employing diuresis as a management approach for
BSD. It is crucial to attain optimal management of nephrotic syndrome to
minimize the risk of BSD, considering the ongoing fluid shifts and the
chronic use of corticosteroid. Future research is needed to enhance the
understanding of the underlying pathogenesis of BSD. Additionally,
further clinical trials are imperative to thoroughly assess the efficacy
of diuresis as a viable management approach for BSD in order to
establish the optimal management approaches for treating the condition.
By shedding light on this barely explored area, the novelty of our
findings contributes to enhancing the understanding of the potential
therapeutic options for addressing bullous stria distensa.

\textbf{Conclusion:}

To conclude, the dramatic appearance of the fluid-filled striae distensa
may cause concerns among physicians who may not be familiar with this
uncommon presentation, although they are benign. The emergence of
bullous lesions in this context is likely attributed to the chronic use
of systemic steroids and the underlying connective tissue weakening
associated with the stria. Therefore, awareness of this rare
complication and unusual clinical presentation is fundamental to prevent
unnecessary investigations or treatments and ensure appropriate
management of the underlying condition.

\textbf{References:}

\begin{enumerate}
\tightlist
\item
  Ross NA, Ho D, Fisher J, et al. Striae Distensae: Preventative and
  Therapeutic Modalities to Improve Aesthetic Appearance. Dermatologic
  surgery : official publication for American Society for Dermatologic
  Surgery {[}et al{]}. 2017;43(5):635-648.
\item
  Gupta V, Yadav S. Bullous striae distensae. Postgraduate medical
  journal. 2017;93(1096):108.
\item
  Seshadri D, De D, Rathi M, George J, J Kanwar A. Fluid Within Striae
  -- An Unusual Phenomenon. Vol 32013.
\item
  Jogova M, Hwang SW. Fluid-filled striae in a patient with
  hypoalbuminemia. CMAJ : Canadian Medical Association Journal.
  2017;189(28):E942-E942.
\item
  Lee JH, Lee EK, Kim CW, Kim TY. A case of edematous striae distensae
  in lupus nephritis. J Dermatol. 1999 Feb;26(2):122-4. doi:
  10.1111/j.1346-8138.1999.tb03523.x. PMID: 10091484.
\item
  Masood S, Jalil P, Naveed S, Kanwal S. Bullous Striae Distensae with
  Prolonged Steroid Use: An Unusual Clinical Presentation.~Indian
  Dermatol Online J. 2020;11(2):280-281. Published 2020 Mar 9.
  doi:10.4103/idoj.IDOJ\_239\_19
\item
  Almashat SA, Adas A. Infected Edematous Striae Distensae. J Clin Exp
  Dermatol Res. S. 2021;11:577.
\item
  Liu C, Sutherland R. Yellow bullous striae distensae. Indian J
  Dermatol Venereol Leprol. 2022 Nov 8:1-2. doi:
  10.25259/IJDVL\_699\_2022. Epub ahead of print. PMID: 36461807.
\item
  Tabri F. Severe striae and steroid acne as side effects caused by
  long-term systemic corticosteroid treatment: A case report and review
  of the literature. Int J Med Rev Case Rep. 2019;3(5):247-54.
\item
  Cho C, Cho E, Kim N, Shin J, Woo S, Lee J, et al. Biophysical
  properties of striae rubra and striae alba in human skin: Comparison
  with normal skin. Skin Res Technol. 2019;25(3):283-288.
\end{enumerate}

Tables

\textbf{Table 1:} Main findings from literature review addressing each
of the selected domains.\selectlanguage{english}
\begin{longtable}[]{@{}lllllll@{}}
\toprule
\begin{minipage}[b]{0.12\columnwidth}\raggedright\strut
\textbf{Title}\strut
\end{minipage} & \begin{minipage}[b]{0.12\columnwidth}\raggedright\strut
\textbf{Authors}\strut
\end{minipage} & \begin{minipage}[b]{0.12\columnwidth}\raggedright\strut
\textbf{Age (years), Gender}\strut
\end{minipage} & \begin{minipage}[b]{0.12\columnwidth}\raggedright\strut
\textbf{Comorbidities}\strut
\end{minipage} & \begin{minipage}[b]{0.12\columnwidth}\raggedright\strut
\textbf{Cutaneous Findings}\strut
\end{minipage} & \begin{minipage}[b]{0.12\columnwidth}\raggedright\strut
\textbf{Investigation Findings}\strut
\end{minipage} & \begin{minipage}[b]{0.12\columnwidth}\raggedright\strut
\textbf{Management Plan}\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Bullous striae distensae\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Vishal Gupta et al. 2016. \textsuperscript{2}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
17, female\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Nephrotic syndrome\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
multiple striae on the axillae, abdomen, lower back, buttocks and
thighs. The striae on the flanks and lower abdomen appeared to be
swollen and shiny, and clear serous fluid came out from them on
puncturing with a sterile needle\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Proteinuria +4 Anaemia Hypoalbuminemia\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Not mentioned\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Fluid Within Striae - An Unusual Presentation\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Divya Seshadri et al. 2013. \textsuperscript{3}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
14, female\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Nephrotic syndrome\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Swollen, bulged out shiny, translucent abdominal striae\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
High urine albumin Hypoalbuminemia\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Not mentioned\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Fluid-filled striae in a patient with hypoalbuminemia\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Maria Jogova et al. 2017. \textsuperscript{4}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
57, female\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Protein losing enteropathy secondary to C. Difficile Infection\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
numerous linear, lobulated, fluid-filled skin lesions that flattened
with transient pressure on the limbs and trunk\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Hypoalbuminemia High urine protein\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Antibiotics Diuresis\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
A Case of Edematous Striae Distensae in Lupus Nephritis\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Lee JH et al. 1998. \textsuperscript{5}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
17, female\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
SLE (lupus nephritis)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Painful edematous Striae distensae on the abdomen.\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Speckled ANA\textsuperscript{+} Positive Anti-dsDNA\textsuperscript{+}
Positive SSA\textsuperscript{+} antigen Positive ENA\textsuperscript{+}
antigen Low Serum C3\textsuperscript{*} levels Proteinuria +3
Hypoalbuminemia\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
400 mg/day of furosemide 62.5 mg/day of systemic
methylprednisolone\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Bullous Striae Distensae with Prolonged Steroid Use: An Unusual Clinical
Presentation\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Sadia Masood et al. 2020. \textsuperscript{6}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
28, female\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Pregnant with SLE\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Abdominal and breast striae with fluids\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Positive ANA\textsuperscript{+} Positive
anti-dsDNA\textsuperscript{+}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
400 mg hydroxychloroquine along with SLE medications.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Infected Edematous Striae Distensae\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Salma Ahmad Almashat et al. 2021.\textsuperscript{7}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
13, female\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Nephrotic syndrome\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Diffuse abdominal redness and distention with fluid-filled striae\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
High White Blood cell count (WBC) High D-dimer Hypoalbuminemia High
urine protein\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Amoxicillin 1 gram (bis in die) BID; Twice a day.\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Yellow bullous striae distensae\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Chaocheng Liu et al. 2022. \textsuperscript{8}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
25, male\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Dermatomyositis with liver dysfunction\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
yellow linear bullous eruption over his inner arms\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Hypoalbuminemia Elevated liver function tests (LFTs)\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Not Mentioned\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
\textbf{Bullous Striae Distensae: First Case Report in The Middle East
of a Rare Presentation (current case)}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Alrefaie~et al. 2023\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
17, female\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Nephrotic Syndrome\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Multiple translucent bullae along the striae distribution on her abdomen
and extending to the flanks\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
hypoproteinaemia abnormal lipid profile anaemia neutrophilic
leucocytosis lymphopenia thrombocytosis hypocalcaemia high
microalbumin/creatinine ratio abnormal urine analysis Fluid aspiration:
-Fluid albumin level was 0.3. -WBC count was 42
cells\textbackslash{}mm\textsuperscript{3}\strut
\end{minipage} & \begin{minipage}[t]{0.14\columnwidth}\raggedright\strut
Diuresis\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

\textsuperscript{+}Note: ANA: Antinuclear Antibody Test, Anti-dsDNA:
Anti-double stranded DNA antibodies, SSA antigen:
Sj\selectlanguage{ngerman}ögren's-syndrome-related antigen, ENA antigen: Extractable nuclear
antigen, C3\textsuperscript{*} levels: complement (C3) levels.

Table 2: Abnormal Laboratory Results\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Test/Parameter\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
\textbf{Result}\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
\textbf{Normal Values}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Complete Blood Count (CBC)\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Complete Blood Count (CBC)\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Complete Blood Count (CBC)\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
Haemoglobin (Hb)\strut
\end{minipage} & \begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
9.0 g/dL\strut
\end{minipage} & \begin{minipage}[t]{0.32\columnwidth}\raggedright\strut
Male:13.8-17.2 g/dL Female: 12.1 - 15.1 g/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
White Blood Cells (WBC)\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
22.1 cells/mm\textsuperscript{3}\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
4,500-11,000 cells/mm\textsuperscript{3}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Neutrophil\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
20.48 k/uL\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
4.5 -- 11.0 K/uL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Lymphocytes\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
1.00 k/uL\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
1.5-6.8 K/uL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Platelets\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
541*10\textsuperscript{9}/L\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
150 - 400 \selectlanguage{ngerman}× 10\textsuperscript{9}/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Lipid Profile\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Lipid Profile\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Lipid Profile\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Cholesterol\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
6.9 mmol/L\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
\textless{} 5.2 mmol/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Low Density Lipoprotein (LDL)\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
4.01 mmol/L\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
\textless{}2.6 mmol/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Triglycerides\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
2.63 mmol/L\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
\textless{} 1.7 mmol/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Liver Function Test\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Liver Function Test\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Liver Function Test\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Total Protein\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
44 g/dL\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
6.0 - 8.3 g/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Albumin\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
5 g/dL\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
3.4 - 5.4 g/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Fluid Culture\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Fluid Culture\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Fluid Culture\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Fluid Albumin\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
0.3 g/dL\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
3.5-5.5 g/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Chemistry\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Chemistry\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Chemistry\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Calcium (Ca\textsuperscript{2+})\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
1.91 mmol/L\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
2.2 - 2.7 mmol/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Urine analysis\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Urine analysis\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Urine analysis\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
RBCs\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
152 RBC / HPF\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
\textless{}4 RBC/HPF\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Kidney function tests\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Kidney function tests\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Kidney function tests\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
microalbumin/creatinine ratio\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
10380.9000 mg/g\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
\textless{} 30 mg/g\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Histopathology\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Histopathology\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Histopathology\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
Punch biopsy of the lesions\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
oedematous dermis with relatively thinned horizontally oriented dermal
collagen.\strut
\end{minipage} & \begin{minipage}[t]{0.30\columnwidth}\raggedright\strut
oedematous dermis with relatively thinned horizontally oriented dermal
collagen.\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

\textbf{Hosted file}

\verb`figure BSD 2.docx`  available at \url{https://authorea.com/users/699964/articles/687058-bullous-striae-distensae-in-a-nephrotic-syndrome-patient-a-case-report-of-a-rare-presentation-and-review-of-the-literature}

\selectlanguage{english}
\FloatBarrier
\end{document}

